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Main Classes of Drugs
Published in Jerome Z. Litt, Neil H. Shear, Litt's Drug Eruption & Reaction Manual, 2017
ACE inhibitorBenazeprilCaptoprilCilazaprilEnalaprilFosinoprilImidaprilLisinoprilMoexiprilPerindoprilQuinaprilRamiprilTrandolaprilZofenopril
Commonly prescribed drugs
Published in Alistair Burns, Michael A Horan, John E Clague, Gillian McLean, Geriatric Medicine for Old-Age Psychiatrists, 2005
Alistair Burns, Michael A Horan, John E Clague, Gillian McLean
Angiotensin-converting enzyme inhibitors (ACEIs) inhibit the conversi�n of angiotensin I to angiotensin II (captopril, cilazapril, enalapril maleate, fos- inopril, imidapril, lisinopril, moexipril hydrochloride, perindopril, quinapril, ramipril and trandolapril).
Pneumonia
Published in Thomas T. Yoshikawa, Shobita Rajagopalan, Antibiotic Therapy for Geriatric Patients, 2005
Mutsuo Yamaya, Hidetada Sasaki
An angiotensin-converting enzyme (ACE) inhibitor inhibits an enzyme to metabolize substance P. By administering an ACE inhibitor, the small amount of substance P in the pharynx or trachea will remain there and not be metabolized. The concentration of substance P increases with time, and this will, in turn, return the swallowing/coughing reflex to normal. With an ACE inhibitor, the side effect of coughing is three times more likely to happen in women than in men. When the ACE inhibitor imi-dapril was administered for 2 years, the incidence of pneumonia was reduced to one-third, compared with a group to which no imidapril was administered (1). The high risk factor of silent aspiration for CAP is confirmed by the fact that interventions to prevent silent aspiration decrease the incidence of CAP in older people.
Angiotensin converting enzyme and angiotensin converting enzyme inhibitors in dermatology: a narrative review
Published in Expert Review of Clinical Pharmacology, 2022
A literature search was conducted in PubMed, Embase and Google Scholar for relevant studies from 1985 to 5 July 2021 using the index words, ‘angiotensin converting enzyme inhibitors,’ ‘angiotensin II receptor blockers,’ ‘renin angiotensin system’ and the co-indexing terms ‘treatment,’ ‘captopril,’ ‘enalapril,’ ‘lisinopril,’ ‘ramipril,’ ‘perindopril,’ ‘trandolapril,’ ‘benazepril,’ ‘quinapril,’ ’fosinopril’, ‘imidapril,’ ‘zofenopril,’ ‘cilazapril,’ ‘moexipril,’ ‘cutaneous reaction’ and ‘dermatology.’ This review article was divided into three parts. The first part discusses the clinical use of ACEI in dermatology (Table 1, 2) (Figure 1). The second part describes the relationship between ACE and immune diseases, and further discusses the possible relationship between the clinical use of ACEI for these diseases and ACE (Table 3). The third part focuses on the cutaneous adverse reactions of ACEI.
New perspectives on the definition, diagnosis, and treatment of true arterial hypertension
Published in Expert Opinion on Pharmacotherapy, 2020
Ramón C. Hermida, Michael H. Smolensky, Artemio Mojón, Juan J. Crespo, María T. Ríos, Manuel Domínguez-Sardiña, Alfonso Otero, José R. Fernández
A vast number of clinical trials demonstrate ingestion of ACEI medications of different terminal half-life – benazepril, captopril, enalapril, imidapril, lisinopril, perindopril, quinapril, ramipril, spirapril, trandolapril, and zofenopril – in the evening/bedtime compared to upon awakening results in significantly better: (i) attenuated asleep than awake BP mean, (ii) transformation of the 24 h BP profile toward normal dipper one, and (iii) patient tolerance to treatment, i.e. decreased incidence of adverse effects [21–24,26,29]. Additionally, many prospective randomized trials involving the ARB medications of irbesartan, olmesartan, telmisartan, and valsartan validate identical significant ingestion-time differences in therapeutic effects as ACEIs, also independent of medication terminal half-life [21,23,24,29]. Moreover, bedtime dosing of valsartan [56], candesartan [57,58], and olmesartan [59] significantly decreases urinary albumin level in an amount strongly correlated with extent of treatment-induced reduction of asleep BP mean and increase of sleep-time relative BP decline [56], and, as reported in one study, with improved baroreflex sensitivity [58].
Thymosin-β4: A key modifier of renal disease
Published in Expert Opinion on Biological Therapy, 2018
Elisavet Vasilopoulou, Paul R. Riley, David A. Long
Subsequent studies explored the therapeutic effect of Ac-SDKP in combination with ACE inhibitors in diabetic nephropathy. Combination treatment with Ac-SDKP (500 μg/kg/day) and the ACE inhibitor, Imidapril, in male CD1 mice with STZ-induced type I diabetes was initiated 16 weeks post-STZ injection and was maintained for 8 weeks. Combination treatment suppressed glomerular mesangial area expansion, fibrosis, and reduced the ratio of αSMA-positive to CD31+ cells compared with Imidapril alone [63]. The authors explored the possibility that Ac-SDKP blocks endothelial to mesenchymal transition (EndMT), which has been proposed as a mechanism that contributes to glomerulosclerosis in early diabetic nephropathy [64], and found evidence that Ac-SDKP inhibits EndMT of human dermal microvascular endothelial cells in vitro [63]. In addition, the effect of Ac-SDKP on the expression of microRNAs downregulated in mouse models of CKD and proposed to reduce fibrosis by targeting TGF-β signaling [65,66] was explored. Treatment with Ac-SDKP alone (500 μg/kg/day for 8 weeks initiated 16 weeks post-STZ administration) [67] or Imidapril and Ac-SDKP [63,68] restored the expression of anti-fibrotic microRNAs, miR-29, and miR-let-7, in the diabetic kidney.